I happened to save which includes unsealed docs from some of the states. Some of these people could be included in the sealed docs but for whatever reason (listed in the report above) are unsealed.
I still have to ask, how did they know? I don't see a differentiation here. Enlighten me. I read the report and I know the OP said criminal were 1077, then jumped to the current #. The 2009 report done for 2006 differentiated between criminal and civil but they spoke to people in the court system for the study.
Sorry to be a pain. Either or, this is highly unusual.
Hopefully the media will be alert on Monday morning, and keeping an eye on the Federal courthouses.
You aren't being a pain. There is no way to verify with this list (or any other really) unless we had PACER access to verify.
Clearly, we cannot confirm from the truncated list as tweeted, so I am just pointing to what one of the compilers wrote who claims to be a legal professional.
Thanks MME, that helps. I haven't been back to see replies. My question about civil vs criminal was picky because even if the ratio were the same, the # sealed is still unprecedented for less than a month compared to a year, even if a years worth has doubled since 2006. Something is happening and most of us are hoping it is a swamp draining.
Just so we are clear that is 1.9 cases per district court per day. Of course not all districts see the same amount. Somewill see more or less then average. So I dont think this is the big coup the right have been raving about since Mueller started his indictments.
Yes, either way it does appear to be an unusually high amount. More so if it is only sealed criminal cases/indictments/matters.
Maybe the trump DOJ not wanting people to see all the charges he and his company has beaten over the years??
.. that is me reaching big time though..
Maybe someone trying to erase some previous charge and not wanting to publicly admit it, so they did thousands .. It's too many charges to be something targeted..


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Thread: Does the BCWF intend to weigh in on the suggested handgun and 'assault weapons' ban?
Honestly, gun laws are not what the bcwf need spend much time and effort in.
Firstly, I think there are enough "gun affiliated lobbyists" running around already to make sure it doesn't happen.
BCWF to be focused on.
Lets face it, BCWF is going thru a period right now, that if they don't get their act together real quick, it is going to be the end of BCWF in the not to distant future by many members walking away from their memberships.
May want to call up the NRA etc to send some folks up for the gun issues.
I think they should. Why ? Because the current Goberment is saying only FN, hunters and farmers should be able to use guns. Who better to talk about that than the BCWF ? Stop this division, all orgs need to jump on this.
The end game is bigger than people think IMO. I keep seeing threads about the next hunting trip, well if Blair gets his way with CENTRAL STORAGE FOR ALL GUNS have fun trying to hunt on the fly.


We are a church who has deliberately chosen to build its people through expositional preaching with a Christ-centered approach. What that means is that the messages you hear preached at First Southern will typically work through a particular bible passage verse by verse in order to declare the truth of the text and to apply it to everyday life. The preaching is Christ-centered in that the bible is always interpreted in light of the grand story of redemption through Jesus Christ.
Each time we preach, it is our goal to connect with every listener, declare the truth, allow the Holy Spirit to bring conviction, and consider how we might live out that declared truth in everyday life. It is a very simple approach but we believe that God is using it to transform his people. For that we are grateful! You are encouraged to listen to the sermons below and wrestle deeply with what the Holy Spirit may be saying to you. May you be changed by the word of God.


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We work very hard to bring you locally grown blooms for much of the year. But you can always be assured that your bouquet is all American grown. Which is why our bouquets look different. As in: not cheesy, just picked, garden style, hand tied, slow flowers. And they are eco friendly too, so pat yourself on the back. You did a super good thing by ordering flowers from us!
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text:
CFLAGS = -Wall -g -std=gnu99 -pthread -DSTEPPER_WARNINGS -DGPIO_WARNINGS
CC=clang
LIBS = -lm -lrt

all: stepper_control

stepper_control: main.c libstepper.so
	$(CC) $(CFLAGS) main.c -fPIC -o stepper_control $(LIBS) -L. -lstepper

libstepper.so: gpio.o stepper.o threaded_stepper.o
	$(CC) -shared gpio.o stepper.o threaded_stepper.o -o libstepper.so $(LIBS)

threaded_stepper.o: threaded_stepper.c threaded_stepper.h
	$(CC) $(CFLAGS) -fPIC -c threaded_stepper.c -o threaded_stepper.o

stepper.o: stepper.c stepper.h
	$(CC) $(CFLAGS) -fPIC -c stepper.c -o stepper.o

gpio.o: gpio.c gpio.h
	$(CC) $(CFLAGS) -fPIC -c gpio.c -o gpio.o

clean:
	rm -f *.o stepper_control libstepper.so

redpajama_set_name: RedPajamaGithub


text:
package main

import (
	certcenter "certcenter.com/go"
	"fmt"
	_ "io/ioutil"
	_ "time"
)

// Set your valid OAuth2 Bearer
// (see https://developers.certcenter.com/docs/authentication)

func init() {
	certcenter.Bearer = "AValidToken.oauth2.certcenter.com"
}

func main() {
	// DeleteVoucher allows you to invalidate a particular voucher
	// https://developers.certcenter.com/v1/reference#deletevoucher
	//
	res, _ := certcenter.DeleteVoucher(&certcenter.DeleteVoucherRequest{VoucherCode: "JDX1UBHC6UA3"})
	fmt.Println(res)
	return
}


As Panchenko observes, not one of the travel journals Prostitutes the participants on the excursion Kaniv a single mention of anything like this. Help Center Find new research Kaniv in: I can Prostitutes you her Prostituutes page.
Valerii Smolii Kyiv: I have been dating a lady from Cherkasy City for 8 month now, she told me her life story. Methuen, New Accents, , No ships or fortresses? My father put some corncobs under the roof.
Reikartz Attache Kyiv Kiev. I know her first name and date of birth, and the name of her daughter.
Most likely it is the case that women, due to shame, guilt, or trauma, preferred to keep silent. They were especially struck by the shipyards, which launched their first ships in the presence of these Kaniv. Viola, Peasant Rebels under Stalin, — Because it cannot address all the issues, this fact could partially justify my decision.
I knew all the scams by then, and saw this as part of a probable scam.
Panchenko got to the bottom of this myth.
I have some personal details about her, area of residence, work and more.
She managed to meet Petrovsky and get an order that the local authorities return our house and all our belongings … Ultimately, they Prostitutes us nothing back … but a er that they le us alone.
The woman le the child at home and went a er Prostitutes hus- band.


And get back to the business of girning..
and after girning I shall be looking for the best bins to rake in once the Tories have finished their cutting of wages, pensions and conditions.
I disagree with this argument.
If you're a Conservative voter then you should vote no. You may get a greater representation within Scotland, but they would never form the government.
Although I think there's scope for a centre-right party to supercede the Tories after independence that could do very, very well.
It depends whether you believe in most - democracy or getting what you personally want?
It can't be both. If I voted for Tory I'd be extrenely uncomfortable about them ruling my country with a single MP because democracy is the loser there.
When your questions start making sense I'll be happy to respond.
Same. Country full of scaredy cat bawbags if we vote No. Supposed to be a patriotic country too..
You can be patriotic and still vote No. Nothing wrong with loving Scotland, but loving it as part of the union. Alternatively there's nothing wrong with wanting Scotland to be independent but being pragmatic if it's going to affect your own status.
It really depends on the scale of the defeat. I just hope Westminster imposes hardship on us so the No voters realize how stupid they were to stick with the status quo.
You hope that Westminster screws Scotland over in the event of a No vote. Stunning. Absolutely stunning.
As for me? If there is a No vote, I won't be especially disappointed, but will actively campaign and push for comprehensive fiscal devolution to give Scotland more control over its domestic affairs. If no meaningful progress is made within a decade or so, I will support another referendum on independence.
Democratic deficits occur everywhere though. Texas would never vote for the Democrats, yet they still have Obama imposed on them.
Closer to home, the SNP were not democratically elected to rule the people of Eastwood, but as a whole it was decided to re-elect them.
And I think therein lies the issue.
It goes against the grain for many to cast their vote for what are basically selfish reasons.
The UK has been socially ripped apart because of that attitude.
I personally am voting Yes for the generations which come after me.
I'm taking a holistic view of the future Scotland I'd like to see for the betterment of as many Scots as possible.
It depresses me that fellow Scots are going to vote No in their hundreds of thousands for selfish reasons like having an extra £500 in their pockets.
Thatcher was right - there IS no such thing as society anymore.
People just do what's best for themselves - f**k everyone else.
It's the complaining afterwards from those same people as the inevitable consequences of that level of selfishness hit home which angers me.
And when I see what that attitude has done to the weak and vulnerable in my country it makes me sick to my stomach.
It's a Yes for me. It can't be any other way.
Your case. Not "our". I'm a Yes voter.
You are confusing a BETTER system with a PERFECT system and complaining because Scottish Independence gives you the former.
If the people of Eastwood are so fired up about their deficit they should lobby for their own independence from Scotland and I'd support them.
No, what was won with the suggestion that Texas faces a democratic deficit?
We don't live in America.
So you think Texas should be independent?
We will be a laughing stock if we do indeed vote no. The Irish for example had to actually fight for their independence. All we need to do is cross a box in a polling booth.
"Scotland is a brave nation"... "Aye right, they couldn't even vote to remove themselves from England's bosom."
And I suppose you take and extended lunch hour a few times a week to laugh at Quebec?
But are you saying that being 1 voice in 3 million is any different from being 1 voice in 40 million?
Clearly. In excess of 13 times different.
Quebec were a baw hair away from winning, you can then take into consideration the spoiled ballot papers. Very dodgy.
In places like Quebec and Catalonia, independence is arguably more about identity and cultural oppression than politics or economics. To the outside world these places aren't viewed as nations like Scotland is. Our constitutional debate is overwhelmingly about political and economic arguments.
Scotland has not been around for "millennia". It came into existence in the 800s. It is only one millenium old.


you'll help them truly experience it.
Are you ready for anything? Because everything can happen when people travel.
Fulfill all Lifestyle/Concierge requests, i.e., Fine Dining, Tickets to the Theatre/Opera and sporting events, flowers, limousine arrangements etc along with the ability to fulfill any specialized Card Member requests. All fulfillment's must be flawless with the best available options offered to Card members while maintaining accurate and updated personal Card Member details at all times.
Provide extraordinary services to premium Card members that create the personal touch in the course of relationship development. Offer alternate solutions that delight Card members with "Wow" factors and handle their requests with tact and compassion to maximize customer satisfaction.
Remain focus and take ownership when dealing with challenging situations and leverage support from colleagues / superiors. Only escalating calls where it is essential.
Work closely with external vendors or Amex establishment to ensure complete and accurate processing of lifestyle transactions, as well as following the necessary process and protocols as required.
Follow and adhere to all quality guidelines relating to the company scorecard to ensure great customer experience.
Observe productivity standards by fulfilling all requests in a timely and accurate manner in accordance with commitments made to Card members.
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- Applied Filter Forge (Jumble filter).
- Ran the 12-point Kaleidoscope action by MikeW.
- Applied the Spherize filter (Filter>Distort).
- Ran the file through Topaz Studio (AI Remix Adjustment).
- Created the photo sphere effect with a template by LeGraficano.


text:
Tata Motors Achieves the Milestone of Producing 4 Million Passenger Vehicles Press kit
249.85 KB Download
Tata Motors celebrates the landmark achievement of producing 4 million passenger vehicles with #WeLoveYou4Million campaign thanking all its loyal customers.
Tata Motors celebrates the significant milestone of crossing 4 million-production mark with a flag-off ceremony of their 'New Forever' range of passenger vehicles along with the electrifying Nexon EV, from its manufacturing facility in Pune.
Expresses its gratitude towards customers with the 'We Love You 4 Million' campaign
Tata Motors today announced a landmark achievement of producing 4 million passenger vehicles in India, since its inception. The company expresses its gratitude to the tremendous customer support that has made this accomplishment possible. In light of this, Tata Motors has launched the 'We Love You 4 Million' campaign to honour the support of its customers through this successful journey.
Over the years, Tata Motors has produced legendary vehicles like the Indica, Sierra, Sumo, Safari and the Nano that have played a pivotal role in the shaping the country in its post economic liberalisation era. These iconic vehicles have broken barriers across categories in the Indian automobile sector. With the launch of the Tata Safari, the company pioneered the concept of a 'lifestyle SUV' to the industry, thereby creating the most aspirational four-wheeler for its customers. In honour of the legacy of Mr. Sumant Moolgaonkar, Tata Motors introduced the first ever MPV in Tata Sumo. With Indica, the company changed the customer perception in terms of how a passenger vehicle is received. In the more recent past, Tata Motors redefined the entry level car and the compact SUV segment with the rollout of the Tiago and the Nexon respectively.
As of today, with its New Forever BS6 range consisting of the Tiago, Tigor, Nexon, Harrier and the Altroz, the company has the youngest and the safest product portfolio in the market. Tata Motors has been India's first car manufacturer to have received a 5-star Global NCAP rating for its model, the Nexon. Tata Motors is also India's largest EV manufacturer with 67% market share and leading the way on electric vehicle adoption in India.
The company had achieved the 1 million production mark for passenger vehicles in 2005-06, 3 million in 2015 and the 4 million production milestone was achieved this month.
Commenting on this historic event, Mr. Shailesh Chandra – President, Tata Motors Passenger Vehicles Business Unit said, "As India's home-grown automotive brand, we are delighted to have reached this prominent milestone for our passenger vehicles segment. Since its inception, Tata Motors' commitment to introducing products that have the best-in-class safety, design and performance has brought to life the vision of our Chairman Emeritus Mr. Ratan Tata. Over the last 30 years, we have rolled out icons that have not only catered to evolving customer needs but have also set new benchmarks in their respective segments. Our "New Forever" range of passenger vehicles only strengthens our commitment towards our customers. In bid to become future ready we have embarked on a sustainability journey with EVs and are leading India's journey towards sustainable transportation."
In the last 3 decades, the company has not only rolled out class-defining products, but has also significantly evolved in terms of manufacturing and technology. Tata Motors was the first Indian company to develop indigenous capabilities from the design, development, validation and manufacturing stages as well as have a streamlined sales & service operations, all under one umbrella. It was also the first car manufacturer to install a crash test facility in India. As of today, Tata Motors has in-house design and simulation studios that execute rapid prototyping, digital product development, and a fully-equipped emission testing facilities to enhance its engineering capabilities, thereby developing best-in-class products. Tata Motors has state-of-the-art manufacturing facilities at Chikhali, Pune; Sanand in Gujarat; and the FIAPL plant at Ranjangaon in Pune.
Link to the campaign is as follows: https://twitter.com/TataMotors_Cars/status/1319961906916986880?s=19
To know more about offers and car buying options, call your nearest dealership or visit https://cars.tatamotors.com/.
Customers can also enquire, request a test drive, make bookings and select their preferred financing option via the recently launched 'Click to Drive', an end-to-end online platform from the comfort and safety of their homes.
About Tata Motors
Tata Motors Limited (NYSE: TTM; BSE: 500570 and 570001; NSE: TATAMOTORS and TATAMTRDVR), a USD 35 billion organization, is a leading global automobile manufacturer of cars, utility vehicles, pick-ups, trucks and buses. Part of the USD 113 billion Tata group, Tata Motors is India's largest and the only OEM offering extensive range of integrated, smart and e-mobility solutions. It has operations in India, the UK, South Korea, Thailand, South Africa, and Indonesia through a strong global network of 103 subsidiaries, 10 associate companies, 3 joint ventures and 2 joint operations as on March 31, 2020.
With a focus on engineering and tech enabled automotive solutions catering to the future of mobility, Tata Motors is India's market leader in commercial vehicles and amongst the top four in the passenger vehicles market. With 'Connecting Aspirations' at the core of its brand promise, the company's innovation efforts are focused to develop pioneering technologies that are sustainable as well as suited to evolving aspirations of the market and the customers. Tata Motors strives to bring new products that fire the imagination of GenNext customers, fueled by state of the art design and R&D centers located in India, UK, US, Italy and South Korea. Internationally, Tata commercial and passenger vehicles are marketed in countries, spread across Africa, the Middle East, South Asia, South East Asia, South America, Australia, CIS, and Russia.

redpajama_set_name: RedPajamaCommonCrawl


text:
/*jslint sloppy: true, nomen: true */
/*global window:true,phantom:true */

/*
  This file is part of the PhantomJS project from Ofi Labs.

  Copyright (C) 2011 Ariya Hidayat <ariya.hidayat@gmail.com>
  Copyright (C) 2011 Ivan De Marino <ivan.de.marino@gmail.com>
  Copyright (C) 2011 James Roe <roejames12@hotmail.com>
  Copyright (C) 2011 execjosh, http://execjosh.blogspot.com
  Copyright (C) 2012 James M. Greene <james.m.greene@gmail.com>

  Redistribution and use in source and binary forms, with or without
  modification, are permitted provided that the following conditions are met:

    * Redistributions of source code must retain the above copyright
      notice, this list of conditions and the following disclaimer.
    * Redistributions in binary form must reproduce the above copyright
      notice, this list of conditions and the following disclaimer in the
      documentation and/or other materials provided with the distribution.
    * Neither the name of the <organization> nor the
      names of its contributors may be used to endorse or promote products
      derived from this software without specific prior written permission.

  THIS SOFTWARE IS PROVIDED BY THE COPYRIGHT HOLDERS AND CONTRIBUTORS "AS IS"
  AND ANY EXPRESS OR IMPLIED WARRANTIES, INCLUDING, BUT NOT LIMITED TO, THE
  IMPLIED WARRANTIES OF MERCHANTABILITY AND FITNESS FOR A PARTICULAR PURPOSE
  ARE DISCLAIMED. IN NO EVENT SHALL <COPYRIGHT HOLDER> BE LIABLE FOR ANY
  DIRECT, INDIRECT, INCIDENTAL, SPECIAL, EXEMPLARY, OR CONSEQUENTIAL DAMAGES
  (INCLUDING, BUT NOT LIMITED TO, PROCUREMENT OF SUBSTITUTE GOODS OR SERVICES;
  LOSS OF USE, DATA, OR PROFITS; OR BUSINESS INTERRUPTION) HOWEVER CAUSED AND
  ON ANY THEORY OF LIABILITY, WHETHER IN CONTRACT, STRICT LIABILITY, OR TORT
  (INCLUDING NEGLIGENCE OR OTHERWISE) ARISING IN ANY WAY OUT OF THE USE OF
  THIS SOFTWARE, EVEN IF ADVISED OF THE POSSIBILITY OF SUCH DAMAGE.
*/

phantom.__defineErrorSignalHandler__ = function(obj, page, handlers) {
    var signal = page.javaScriptErrorSent;
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            catch (e) {}
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        // Delete the previous handler
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        if (typeof f === 'function') {
            var connector = function(message, stack) {
                var revisedStack = JSON.parse(stack).map(function(item) {
                    return { file: item.url, line: item.lineNumber, function: item.functionName }
                });

                f(message, revisedStack);
            };

            // Store the new handler for reference
            handlers[handlerName] = {
                callback: f,
                connector: connector
            };

            signal.connect(connector);
        }
    });

    obj.__defineGetter__(handlerName, function() {
        var handlerObj = handlers[handlerName];
        return (!!handlerObj && typeof handlerObj.callback === "function" && typeof handlerObj.connector === "function") ?
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};

(function() {
    var handlers = {};
    phantom.__defineErrorSignalHandler__(phantom, phantom.page, handlers);
})();

// TODO: Make this output to STDERR
phantom.defaultErrorHandler = function(message, stack) {
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};

phantom.onError = phantom.defaultErrorHandler;

phantom.callback = function(callback) {
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};

(function() {
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    function joinPath() {
        // It should be okay to hard-code a slash here.
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        function require(request) {
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text:
Wasim Hasan Raja (Punjabi, ) (3 July 1952 – 23 August 2006) was a British Pakistani schoolteacher, match referee, cricket coach and cricketer who played in 57 Test matches and 54 One Day Internationals for the Pakistani national cricket team from 1973 to 1985.

His younger brother, Ramiz Raja, also represented Pakistan in Tests and ODIs, becoming captain of the national side. Another brother, Zaeem Raja, also played first-class cricket, as did his father, Saleem Akhtar.

Early and personal life
Wasim Raja was born in Multan in the Punjab. His father was a high-ranking civil servant. Raja obtained a master's degree in political science from Government College, Lahore. He was captain of the Pakistan Under-19 side.

He settled in London after marrying an Englishwoman, Ann. He studied for a certificate in education from Durham University, and he had a spell teaching geography, mathematics and physical education at Caterham School in Surrey. He was also a coach for the Pakistan Under-19 team, and he was an International Cricket Council match referee in 15 Tests and 34 ODIs from 2002 to 2004.

He died of a heart attack in Marlow, Buckinghamshire, England, in August 2006 while playing cricket for the Surrey over-50s side. He is survived by his wife and his sons, Ali and Ahmad.

Career
During his playing career, Raja was known primarily as a dashing middle-order left-handed batsman, with a characteristically generous backlift and breathtaking stokeplay combining a keen eye with wristy execution. Raja also bowled flat wrist spin with his right hand that was good enough to take 51 wickets in Tests, with his scalps including Clive Lloyd, Roy Fredericks, Glenn Turner and Viv Richards. In all, he played in 250 first-class matches, scoring 11,434 runs at an average of 35.18, including 17 centuries, and taking 558 wickets at an average of 29.05.

His finest hour in Test cricket was the tour to the West Indies in 1976–77, when he topped the Pakistani batting averages with 517 runs at 57.4 and came second in the bowling averages with 7 wickets at 18.7, behind Majid Khan. He also scored 14 sixes in the Test series, setting a record that has been equalled 4 times but still remains the only instance away from home. He top-scored in both innings of the drawn 1st Test in Barbados, to push West Indies to within one wicket of their first loss at Kensington Oval since 1935. In their second innings, Pakistan were reduced to 158–9 by Andy Roberts and Colin Croft, a lead of only 144 just over halfway through the fourth day, but a last-wicket stand of 133 with Wasim Bari set the West Indies a target of 306. At the close of the fifth day, West Indies were 55 runs adrift, on 251–9. West Indies won their next 12 matches at Bridgetown, until they were finally beaten by England in the 4th Test in 1994. He was a cricket teacher at Haslemere Preparatory School from 2004 to 2006. There is a memorial plaque there in his honour. He is also remembered in the northeast of England, playing for Durham CCC, before the county was awarded first-class status.

Book
With Adam Licudi, Cornered Tigers: History of Pakistan's Test Cricket from Abdul Kardar to Wasim Akram, 1997, 300 p.

See also
 List of fatalities while playing cricket

References

See also

 Wasim Raja – A breathtaking strokeplayer, Cricinfo, 23 August 2005
 Only the good die young, Cricinfo, 23 August 2006
Wasim Raja dies playing cricket, Cricinfo, 23 August 2006
Obituary, The Daily Telegraph, 24 August 2006
Obituary, The Times, 24 August 2006
Obituary, The Guardian, 25 August 2006

Pakistan Test cricketers
Pakistan One Day International cricketers
Cricketers at the 1975 Cricket World Cup
Cricketers at the 1979 Cricket World Cup
Cricketers at the 1983 Cricket World Cup
Pakistani cricketers
Lahore cricketers
Sargodha cricketers
National Bank of Pakistan cricketers
Durham cricketers
Northumberland cricketers
Alumni of Durham University
Cricket match referees
1952 births
2006 deaths
Cricketers from Multan
Pakistan International Airlines A cricketers
Lahore Greens cricketers
Punjab University cricketers
Lahore A cricketers
Pakistan Universities cricketers
Lahore City Blues cricketers
Lahore City Whites cricketers
Central Zone (Pakistan) cricketers
Cricket deaths
Government College University, Lahore alumni
St. Anthony's High School, Lahore alumni
Pakistani emigrants to the United Kingdom
Naturalised citizens of the United Kingdom
Schoolteachers from Surrey
Pakistani cricket coaches
British people of Punjabi descent
D. B. Close's XI cricketers

redpajama_set_name: RedPajamaWikipedia


text:
Chronic renal disease, kidney failure, impaired kidney function[1]
Uremic frost on the head in someone with chronic kidney disease
Early: None[2]
Later: Leg swelling, feeling tired, vomiting, loss of appetite, confusion[2]
Heart disease, high blood pressure, anemia[3][4]
Long-term[5]
Diabetes, high blood pressure, glomerulonephritis, polycystic kidney disease[5][6]
Diagnostic method
Blood tests, urine tests[7]
Medications to manage blood pressure, blood sugar, and lower cholesterol, renal replacement therapy, kidney transplant[8][9]
753 million (2016)[1]
1.2 million (2015)[6]
Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months to years.[2][5] Initially there are generally no symptoms; later, symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion.[2] Complications include an increased risk of heart disease, high blood pressure, bone disease, and anemia.[3][4][10]
Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease.[5][6] Risk factors include a family history of chronic kidney disease.[2] Diagnosis is by blood tests to measure the estimated glomerular filtration rate (eGFR), and a urine test to measure albumin.[7] Ultrasound or kidney biopsy may be performed to determine the underlying cause.[5] Several severity-based staging systems are in use.[11][12]
Screening at-risk people is recommended.[7] Initial treatments may include medications to lower blood pressure, blood sugar, and cholesterol.[9] Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are generally first-line agents for blood pressure control, as they slow progression of the kidney disease and the risk of heart disease.[13] Loop diuretics may be used to control edema and, if needed, to further lower blood pressure.[14][9][15] NSAIDs should be avoided.[9] Other recommended measures include staying active, and certain dietary changes such as a low-salt diet and the right amount of protein.[9][16] Treatments for anemia and bone disease may also be required.[17][18] Severe disease requires hemodialysis, peritoneal dialysis, or a kidney transplant for survival.[8]
Chronic kidney disease affected 753 million people globally in 2016: 417 million females and 336 million males.[1] In 2015 it caused 1.2 million deaths, up from 409,000 in 1990.[6][19] The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.[6]
Video explanation
1 Signs and symptoms
2.1 By anatomical location
3 Diagnosis
3.1 Screening
3.2 Ultrasound
3.3 Additional imaging
3.4 Stages
4 Management
4.1 Blood pressure
4.2 Other measures
4.3 Referral to a nephrologist
4.4 Renal replacement therapy
5 Prognosis
6 Epidemiology
6.1 Race
8 Other animals
CKD is initially without symptoms, and is usually detected on routine screening blood work by either an increase in serum creatinine, or protein in the urine. As the kidney function decreases:
Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin–angiotensin system, increasing the risk of developing hypertension and heart failure.
Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost").
Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 ml/min/1.73 m2, at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.[20]
Fluid overload symptoms may range from mild edema to life-threatening pulmonary edema.
Hyperphosphatemia results from poor phosphate elimination in the kidney. Hyperphosphatemia contributes to increased cardiovascular risk by causing vascular calcification.[21] Circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the kidney capacity for phosphate excretion declines which may contribute to left ventricular hypertrophy and increased mortality in people with CKD .[22][23]
Hypocalcemia results from 1,25 dihydroxyvitamin D3 deficiency (caused by high FGF-23 and reduced kidney mass)[24] and resistance to the action of parathyroid hormone.[25] Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D3).[26] Later, this progresses to secondary hyperparathyroidism, kidney osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis.[27]
Changes in mineral and bone metabolism that may cause 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (kidney osteodystrophy); and 3) vascular or other soft-tissue calcification.[10] CKD-mineral and bone disorders have been associated with poor outcomes.[10]
Metabolic acidosis may result from decreased capacity to generate enough ammonia from the cells of the proximal tubule.[20] Acidemia affects the function of enzymes and increases excitability of cardiac and neuronal membranes by the promotion of hyperkalemia.[28]
Anemia is common and is especially prevalent in those requiring haemodialysis. It is multifactoral in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone marrow suppression.
In later stages, cachexia may develop, leading to unintentional weight loss, muscle wasting, weakness and anorexia.[29]
Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.[30]
People with CKD are more likely than the general population to develop atherosclerosis with consequent cardiovascular disease, an effect that may be at least partly mediated by uremic toxins.[31][unreliable medical source?] People with both CKD and cardiovascular disease have significantly worse prognoses than those with only cardiovascular disease.[32]
The three most common causes of CKD in order of frequency as of 2015 are diabetes mellitus, hypertension, and glomerulonephritis.[33] About one of five adults with hypertension and one of three adults with diabetes have CKD. If the cause is unknown, it is called idiopathic.[34]
By anatomical location
Vascular disease includes large vessel disease such as bilateral kidney artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome, and vasculitis.
Glomerular disease comprises a diverse group and is classified into:
Primary glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis)
Secondary glomerular disease such as diabetic nephropathy and lupus nephritis
Tubulointerstitial disease includes drug- and toxin-induced chronic tubulointerstitial nephritis, and reflux nephropathy.
Obstructive nephropathy, as exemplified by bilateral kidney stones and benign prostatic hyperplasia of the prostate gland. Rarely, pinworms infecting the kidney can cause obstructive nephropathy.
Congenital disease such as polycystic kidney disease.
Mesoamerican nephropathy, is "a new form of kidney disease that could be called agricultural nephropathy".[35] A high and so-far unexplained number of new cases of CKD, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugar cane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures[36][37][38][39] of about 36 °C (96 °F) is suspected, as are agricultural chemicals[40]
A 12-lead ECG of a person with CKD and a severe electrolyte imbalance: hyperkalemia (7.4 mmol/l) with hypocalcemia (1.6 mmol/l). The T-waves are peaked and the QT interval is prolonged.
Diagnosis of CKD is largely based on history, examination and urine dipstick combined with the measurement of the serum creatinine level (see above). It is important to differentiate CKD from acute kidney injury (AKI) because AKI can be reversible. One diagnostic clue that helps differentiate CKD from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). In many people with CKD, previous kidney disease or other underlying diseases are already known. A significant number present with CKD of unknown cause.
Screening those who have neither symptoms nor risk factors for CKD is not recommended.[41][42] Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with African American ancestry, those with a history of kidney disease in the past, and subjects who have relatives who had kidney disease requiring dialysis.
Screening should include calculation of the estimated GFR (eGFR) from the serum creatinine level, and measurement of urine albumin-to-creatinine ratio (ACR) in a first-morning urine specimen (this reflects the amount of a protein called albumin in the urine), as well as a urine dipstick screen for hematuria.[43]
The glomerular filtration rate (GFR) is derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship:the higher the creatinine, the lower the GFR. It reflects one aspect of kidney function: how efficiently the glomeruli - the filtering units - work. Normal GFR is 90-120 mLs/min. The units of creatinine vary from country to country. But since the glomeruli make up <5% of the mass of the kidney, the GFR does not indicate all aspects of kidney health and function. This can be done by combining the GFR level with the clinical assessment of the person, including fluid status, and measuring the levels of hemoglobin, potassium, phosphate and parathyroid hormone (PTH).
Kidney ultrasonography is useful for diagnostic and prognostic purposes in chronic kidney disease. Whether the underlying pathologic change is glomerular sclerosis, tubular atrophy, interstitial fibrosis or inflammation, the result is often increased echogenicity of the cortex. The echogenicity of the kidney should be related to the echogenicity of either the liver or the spleen (Figure 22 and Figure 23). Moreover, decreased kidney size and cortical thinning are also often seen and especially when disease progresses (Figure 24 and Figure 25). However, kidney size correlates to height, and short persons tend to have small kidneys; thus, kidney size as the only parameter is not reliable.[44]
Chronic renal disease caused by glomerulonephritis with increased echogenicity and reduced cortical thickness. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.[44]
Nephrotic syndrome. Hyperechoic kidney without demarcation of cortex and medulla.[44]
Chronic pyelonephritis with reduced kidney size and focal cortical thinning. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.[44]
End-stage chronic kidney disease with increased echogenicity, homogenous architecture without visible differentiation between parenchyma and renal sinus and reduced kidney size. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.[44]
Additional imaging
Additional tests may include nuclear medicine MAG3 scan to confirm blood flow and establish the differential function between the two kidneys. Dimercaptosuccinic acid (DMSA) scans are also used in kidney imaging; with both MAG3 and DMSA being used chelated with the radioactive element technetium-99.[45]
Chronic kidney disease (CKD) staging - CKD G1-5 A1-3
glomerular filtration rate (GFR) and albumin/creatinine ratio (ACR)
Normal to mildly increased Moderately increased Severely increased
<30 30-300 >300
G1 Normal 90+ 1 if kidney damage present 1 2
G2 Mildly decreased 60-89 1 if kidney damage present 1 2
G3a Mildly to moderately decreased 45-59 1 2 3
G3b Moderately to severely decreased 30-44 2 3 3
G4 Severely decreased 15-29 3 4+ 4+
G5 Kidney failure <15 4+ 4+ 4+
Numbers 1 - 4 indicates risk of progression as well as frequency of monitoring (number of times a year).
Kidney Disease Improving Global Outcomes - KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease [46]
A glomerular filtration rate (GFR) ≥ 60 ml/min/1.73 m2 is considered normal without chronic kidney disease if there is no kidney damage present.
Kidney damage is defined signs of damage seen in blood, urine, or imaging studies which includes lab albumin/creatinine ratio (ACR) ≥ 30.[47] All people with a GFR <60 ml/min/1.73 m2 for 3 months are defined as having chronic kidney disease.[47]
Protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant.[48]
Stage 1: Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 ml/min/1.73 m2) and persistent albuminuria. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.[47]
Stage 2: Mild reduction in GFR (60–89 ml/min/1.73 m2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.[47]
Stage 3: Moderate reduction in GFR (30–59 ml/min/1.73 m2):.[47] British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral.[48]
Stage 4: Severe reduction in GFR (15–29 ml/min/1.73 m2)[47] Preparation for kidney replacement therapy.
Stage 5: Established kidney failure (GFR <15 ml/min/1.73 m2), permanent kidney replacement therapy,[47] or end-stage kidney disease.
The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation). The condition of individuals with CKD, who require either of the two types of kidney replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), people with advanced stage of CKD (stage 5), who have not yet started kidney replacement therapy, are also referred to as NDD-CKD.
Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD. Control of blood pressure and treatment of the original disease are the broad principles of management.
Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are recommended as first-line agents since they have been found to slow the decline of kidney function, relative to a more rapid decline in those not on one of these agents.[13] They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD.[13] ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD.[13] Aggressive blood pressure lowering decreases peoples risk of death.[49]
Aggressive treatment of high blood lipids is recommended.[50]
A low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start.[51] A tailored low-protein diet, designed for low acidity, may help prevent damage to kidneys for people with CKD.[52]
Anemia - A target hemoglobin level of 9–12 g/dL is recommended;[53][54] raising hemoglobin levels to the normal range has not been found to be of benefit.[55]
Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin.
Replacement of erythropoietin is often necessary in people with advanced disease.[56]
It is unclear if androgens improve anemia.[57]
Calcitriol is recommended for vitamin D deficiency and control of metabolic bone disease.
Phosphate binders are used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease.
Phosphodiesterase-5 inhibitors and zinc may improve sexual dysfunction in men.[30]
Referral to a nephrologist
Guidelines for referral to a nephrologist vary between countries. Most agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m2 is less than 30 ml/min; or decreasing by more than 3 ml/min/year).[58]
It may also be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper education regarding options for kidney replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those people with chronic kidney disease opting for future hemodialysis.
At stage 5 CKD, kidney replacement therapy is usually required, in the form of either dialysis or a kidney transplant.
In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes.[59] Hemodialysis with high-flux dialysis membrane, long or frequent treatment, and increased blood/dialysate flow has improved removal of water-soluble small molecular weight uremic toxins. Middle molecular weight molecules are removed more effectively with hemodialysis using a high-flux membrane, hemodiafiltration and hemofiltration. However, conventional dialysis treatment is limited in its ability to remove protein-bound uremic toxins.[60]
CKD increases the risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure.
Chronic kidney disease results in worse all-cause mortality (the overall death rate) which increases as kidney function decreases.[61] The leading cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.[61][62][63]
While kidney replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected.[64][65] Kidney transplantation increases the survival of people with stage 5 CKD when compared to other options;[66][67] however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis.[68]
People with ESKD are at increased overall risk for cancer.[69] This risk is particularly high in younger people and gradually diminishes with age.[69] Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in people with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved outcomes.[70][71]
About one in ten people have chronic kidney disease. In Canada 1.9 to 2.3 million people were estimated to have CKD in 2008.[55] CKD affected an estimated 16.8% of U.S. adults aged 20 years and older in the period from 1999 to 2004.[72] In 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD.[73]
Chronic kidney disease was the cause of 956,000 deaths globally in 2013, up from 409,000 deaths in 1990.[19]
African Americans, American Indians, Hispanics, and South Asians, particularly those from Pakistan, Sri Lanka, Bangladesh, and India, are at high risk of developing CKD. African Americans are at greater risk due to the number of people affected with hypertension among them. As an example, 37% of ESKD cases in African Americans can be attributed to high blood pressure, compared with 19% among Caucasians.[74] Treatment efficacy also differs between racial groups. Administration of antihypertensive drugs generally halts disease progression in white populations but has little effect in slowing kidney disease among black people, and additional treatment such as bicarbonate therapy is often required.[74] While lower socioeconomic status contributes to the number of people affected with CKD, differences in the number of people affected by CKD are still evident between African Americans and Whites when controlling for environmental factors.[74]
The International Society of Nephrology is an international body representing specialists in kidney diseases.
The National Kidney Foundation is a national organization representing people with chronic kidney diseases and professionals who treat kidney diseases.
The American Kidney Fund is a national nonprofit organization providing treatment-related financial assistance to one of every five people undergoing dialysis each year.
The Renal Support Network is a nonprofit, patient-focused, patient-run organization that provides nonmedical services to those affected by CKD.
The American Association of Kidney Patients is a nonprofit, patient-centric group focused on improving the health and well-being of CKD and people undergoing dialysis .
The Renal Physicians Association is an association representing nephrology professionals.
It was said to be costing the British NHS about £1.5 billion a year in 2020.[75]
The UK National Kidney Federation and British Kidney Patient Association (BKPA) represents people with chronic kidney disease. The Renal Association represents Kidney physicians and works closely with the National Service Framework for kidney disease.
Kidney Health Australia serves that country.
The total rate of CKD in dogs was 16 cases per 10,000 years. The mortality rate of CKD was 10 deaths per 10,000. The breeds with the highest rates were the Bernese mountain dog, miniature schnauzer and boxer. The Swedish elkhound, Siberian husky and Finnish spitz were the breeds with the lowest rates.[76][77]
Currently, several compounds are in development for the treatment of CKD. These include the angiotensin receptor blocker (ARB) olmesartan medoxomil; and sulodexide, a mixture of low molecular weight heparin and dermatan sulfate.[78][79]
Unbiased research with complete reporting is required to determine the safety and effectiveness of acupuncture to treat depression, pain, sleep problems, and uraemic pruritus in people who are undergoing dialysis treatments on a regular basis.[80]
↑ 1.0 1.1 1.2 Bikbov B, Perico N, Remuzzi G (23 May 2018). "Disparities in Chronic Kidney Disease Prevalence among Males and Females in 195 Countries: Analysis of the Global Burden of Disease 2016 Study". Nephron. 139 (4): 313–318. doi:10.1159/000489897. PMID 29791905.
↑ 2.0 2.1 2.2 2.3 2.4 "What Is Chronic Kidney Disease?". National Institute of Diabetes and Digestive and Kidney Diseases. June 2017. Retrieved 19 December 2017.
↑ 3.0 3.1 Liao MT, Sung CC, Hung KC, Wu CC, Lo L, Lu KC (2012). "Insulin resistance in patients with chronic kidney disease". Journal of Biomedicine & Biotechnology. 2012: 691369. doi:10.1155/2012/691369. PMC 3420350. PMID 22919275.
↑ 4.0 4.1 "Kidney Failure". MedlinePlus. Retrieved 11 November 2017.
↑ 5.0 5.1 5.2 5.3 5.4 "What is renal failure?". Johns Hopkins Medicine. Retrieved 18 December 2017.
↑ 6.0 6.1 6.2 6.3 6.4 GBD 2015 Mortality Causes of Death Collaborators (October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi:10.1016/s0140-6736(16)31012-1. PMC 5388903. PMID 27733281.
↑ 7.0 7.1 7.2 "Chronic Kidney Disease Tests & Diagnosis". National Institute of Diabetes and Digestive and Kidney Diseases. October 2016. Retrieved 19 December 2017.
↑ 8.0 8.1 "Kidney Failure". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 11 November 2017.
↑ 9.0 9.1 9.2 9.3 9.4 "Managing Chronic Kidney Disease". National Institute of Diabetes and Digestive and Kidney Diseases. October 2016.
↑ 10.0 10.1 10.2 KDIGO: Kidney Disease Improving Global Outcomes (August 2009). "KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)" (PDF). Kidney Int. 76 (Suppl 113). Archived from the original (PDF) on 2016-12-13.
↑ "Summary of Recommendation Statements". Kidney International Supplements. 3 (1): 5–14. January 2013. doi:10.1038/kisup.2012.77. PMC 4284512. PMID 25598998.
↑ Ferri, Fred F. (2017). Ferri's Clinical Advisor 2018 E-Book: 5 Books in 1. Elsevier Health Sciences. pp. 294–295. ISBN 9780323529570.
↑ 13.0 13.1 13.2 13.3 Xie X, Liu Y, Perkovic V, Li X, Ninomiya T, Hou W, et al. (May 2016). "Renin-Angiotensin System Inhibitors and Kidney and Cardiovascular Outcomes in Patients With CKD: A Bayesian Network Meta-analysis of Randomized Clinical Trials". American Journal of Kidney Diseases (Systematic Review & Meta-Analysis). 67 (5): 728–41. doi:10.1053/j.ajkd.2015.10.011. PMID 26597926.
↑ Wile D (September 2012). "Diuretics: a review". Annals of Clinical Biochemistry. 49 (Pt 5): 419–31. doi:10.1258/acb.2011.011281. PMID 22783025.
↑ James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. (February 2014). "2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8)". JAMA. 311 (5): 507–20. doi:10.1002/14651858.CD011339.pub2. PMC 6485696. PMID 24352797.
↑ "Eating Right for Chronic Kidney Disease | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 5 September 2019.
↑ "Anemia in Chronic Kidney Disease". National Institute of Diabetes and Digestive and Kidney Diseases. July 2016. Retrieved 19 December 2017.
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↑ 19.0 19.1 GBD 2013 Mortality Causes of Death Collaborators (January 2015). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 385 (9963): 117–71. doi:10.1016/S0140-6736(14)61682-2. PMC 4340604. PMID 25530442. Table 2, p. 137
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↑ Bacchetta J, Sea JL, Chun RF, Lisse TS, Wesseling-Perry K, Gales B, et al. (January 2013). "Fibroblast growth factor 23 inhibits extrarenal synthesis of 1,25-dihydroxyvitamin D in human monocytes". Journal of Bone and Mineral Research. 28 (1): 46–55. doi:10.1002/jbmr.1740. PMC 3511915. PMID 22886720.
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↑ 30.0 30.1 Vecchio M, Navaneethan SD, Johnson DW, Lucisano G, Graziano G, Saglimbene V, et al. (December 2010). "Interventions for treating sexual dysfunction in patients with chronic kidney disease" (PDF). The Cochrane Database of Systematic Reviews (12): CD007747. doi:10.1002/14651858.CD007747.pub2. PMID 21154382.
↑ Hoyer, FF; Nahrendorf, M (2 January 2019). "Uremic Toxins Activate Macrophages". Circulation. 139 (1): 97–100. doi:10.1161/CIRCULATIONAHA.118.037308. PMC 6394415. PMID 30592654.
↑ Damman K, Valente MA, Voors AA, O'Connor CM, van Veldhuisen DJ, Hillege HL (February 2014). "Renal impairment, worsening renal function, and outcome in patients with heart failure: an updated meta-analysis". European Heart Journal. 35 (7): 455–69. doi:10.1093/eurheartj/eht386. PMID 24164864.
↑ GBD 2015 Disease Injury Incidence Prevalence Collaborators (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
↑ "United States Renal Data System (USRDS)". Archived from the original on 2007-02-13.
↑ Orantes CM, Herrera R, Almaguer M, Brizuela EG, Núñez L, Alvarado NP, et al. (April 2014). "Epidemiology of chronic kidney disease in adults of Salvadoran agricultural communities". MEDICC Review. 16 (2): 23–30. PMID 24878646.
↑ Tangri N (29 July 2013). "MesoAmerican Nephropathy: A New Entity". eAJKD. National Kidney Foundation.
↑ Wesseling C, Crowe J, Hogstedt C, Jakobsson K, Lucas R, Wegman DH (November 2013). "The epidemic of chronic kidney disease of unknown etiology in Mesoamerica: a call for interdisciplinary research and action". American Journal of Public Health. 103 (11): 1927–30. doi:10.2105/AJPH.2013.301594. PMC 3828726. PMID 24028232.
↑ Johnson RJ, Sánchez-Lozada LG (October 2013). "Chronic kidney disease: Mesoamerican nephropathy--new clues to the cause". Nature Reviews. Nephrology. 9 (10): 560–1. doi:10.1038/nrneph.2013.174. PMID 23999393.
↑ Roncal Jimenez CA, Ishimoto T, Lanaspa MA, Rivard CJ, Nakagawa T, Ejaz AA, et al. (August 2014). "Fructokinase activity mediates dehydration-induced renal injury". Kidney International. 86 (2): 294–302. doi:10.1038/ki.2013.492. PMC 4120672. PMID 24336030.
↑ Chavkin, Sasha; Greene, Ronnie (12 December 2011). "Thousands of sugar cane workers die as wealthy nations stall on solutions". International Consortium of Investigative Journalists. Retrieved November 26, 2012.
↑ Qaseem A, Hopkins RH, Sweet DE, Starkey M, Shekelle P (December 2013). "Screening, monitoring, and treatment of stage 1 to 3 chronic kidney disease: A clinical practice guideline from the American College of Physicians". Annals of Internal Medicine. 159 (12): 835–47. doi:10.7326/0003-4819-159-12-201312170-00726. PMID 24145991.
↑ Weckmann GF, Stracke S, Haase A, Spallek J, Ludwig F, Angelow A, et al. (October 2018). "Diagnosis and management of non-dialysis chronic kidney disease in ambulatory care: a systematic review of clinical practice guidelines". BMC Nephrology. 19 (1): 258. doi:10.1186/s12882-018-1048-5. PMC 6180496. PMID 30305035.
↑ Johnson, David (2011-05-02). "Chapter 4: CKD Screening and Management: Overview". In Daugirdas, John (ed.). Handbook of Chronic Kidney Disease Management. Lippincott Williams and Wilkins. pp. 32–43. ISBN 978-1-58255-893-6.
↑ 44.0 44.1 44.2 44.3 44.4 Content initially copied from: Hansen KL, Nielsen MB, Ewertsen C (December 2015). "Ultrasonography of the Kidney: A Pictorial Review". Diagnostics. 6 (1): 2. doi:10.3390/diagnostics6010002. PMC 4808817. PMID 26838799. (CC-BY 4.0)
↑ "Kidney scans". Singlehealth.
↑ CKD Evaluation and Management 2012. Kidney Disease Improving Global Outcomes (KDIGO). Retrieved 2019-07-06.
↑ 47.0 47.1 47.2 47.3 47.4 47.5 47.6 National Kidney Foundation (2002). "K/DOQI clinical practice guidelines for chronic kidney disease". Archived from the original on 2005-04-15. Retrieved 2008-06-29.
↑ 48.0 48.1 National Institute for Health and Clinical Excellence. Clinical guideline 73: Chronic kidney disease. London, 2008.
↑ Malhotra R, Nguyen HA, Benavente O, Mete M, Howard BV, Mant J, et al. (October 2017). "Association Between More Intensive vs Less Intensive Blood Pressure Lowering and Risk of Mortality in Chronic Kidney Disease Stages 3 to 5: A Systematic Review and Meta-analysis". JAMA Internal Medicine. 177 (10): 1498–1505. doi:10.1001/jamainternmed.2017.4377. PMC 5704908. PMID 28873137.
↑ Chauhan V, Vaid M (November 2009). "Dyslipidemia in chronic kidney disease: managing a high-risk combination". Postgraduate Medicine. 121 (6): 54–61. doi:10.3810/pgm.2009.11.2077. PMID 19940417.
↑ Kalantar-Zadeh K, Fouque D (November 2017). "Nutritional Management of Chronic Kidney Disease". The New England Journal of Medicine. 377 (18): 1765–1776. doi:10.1056/NEJMra1700312. PMID 29091561.
↑ Passey C (May 2017). "Reducing the Dietary Acid Load: How a More Alkaline Diet Benefits Patients With Chronic Kidney Disease". J Ren Nutr (Review). 27 (3): 151–160. doi:10.1053/j.jrn.2016.11.006. PMID 28117137.
↑ Locatelli F, Aljama P, Canaud B, Covic A, De Francisco A, Macdougall IC, et al. (September 2010). "Target haemoglobin to aim for with erythropoiesis-stimulating agents: a position statement by ERBP following publication of the Trial to reduce cardiovascular events with Aranesp therapy (TREAT) study". Nephrology, Dialysis, Transplantation. 25 (9): 2846–50. doi:10.1093/ndt/gfq336. PMID 20591813.
↑ Clement FM, Klarenbach S, Tonelli M, Johnson JA, Manns BJ (June 2009). "The impact of selecting a high hemoglobin target level on health-related quality of life for patients with chronic kidney disease: a systematic review and meta-analysis". Archives of Internal Medicine. 169 (12): 1104–12. doi:10.1001/archinternmed.2009.112. PMID 19546410.
↑ 55.0 55.1 Levin A, Hemmelgarn B, Culleton B, Tobe S, McFarlane P, Ruzicka M, et al. (November 2008). "Guidelines for the management of chronic kidney disease". CMAJ. 179 (11): 1154–62. doi:10.1503/cmaj.080351. PMC 2582781. PMID 19015566.
↑ "Anaemia management in people with chronic kidney disease (CG114)". NICE Clinical Guideline. UK National Institute for Health and Care Excellence. February 2011.
↑ journal|last1=Yang|first1=Q|last2=Abudou|first2=M|last3=Xie|first3=XS|last4=Wu|first4=T|title=Androgens for the anaemia of chronic kidney disease in adults.|journal=The Cochrane Database of Systematic Reviews|date=Oct 9, 2014|volume=10|issue=10|pages=CD006881|pmid=25300168|doi=10.1002/14651858.CD006881.pub2}}
↑ "CKD Stage 4". davita.
↑ Vanholder R, De Smet R, Glorieux G, Argilés A, Baurmeister U, Brunet P, et al. (May 2003). "Review on uremic toxins: classification, concentration, and interindividual variability". Kidney International. 63 (5): 1934–43. doi:10.1046/j.1523-1755.2003.00924.x. PMID 12675874.
↑ Yamamoto, Suguru; Kazama, Junichiro James; Wakamatsu, Takuya; Takahashi, Yoshimitsu; Kaneko, Yoshikatsu; Goto, Shin; Narita, Ichiei (14 September 2016). "Removal of uremic toxins by renal replacement therapies: a review of current progress and future perspectives". Renal Replacement Therapy. 2 (1). doi:10.1186/s41100-016-0056-9.
↑ 61.0 61.1 Perazella MA, Khan S (March 2006). "Increased mortality in chronic kidney disease: a call to action". The American Journal of the Medical Sciences. 331 (3): 150–3. doi:10.1097/00000441-200603000-00007. PMID 16538076.
↑ Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J, Culleton B, Hamm LL, et al. (October 2003). "Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention". Circulation. 108 (17): 2154–69. doi:10.1161/01.CIR.0000095676.90936.80. PMID 14581387.
↑ Tonelli M, Wiebe N, Culleton B, House A, Rabbat C, Fok M, et al. (July 2006). "Chronic kidney disease and mortality risk: a systematic review". Journal of the American Society of Nephrology. 17 (7): 2034–47. doi:10.1681/ASN.2005101085. PMID 16738019.
↑ Heidenheim AP, Kooistra MP, Lindsay RM (2004). Quality of life. Contrib Nephrol. Contributions to Nephrology. 145. pp. 99–105. doi:10.1159/000081673. ISBN 978-3-8055-7808-0. PMID 15496796.
↑ de Francisco AL, Piñera C (January 2006). "Challenges and future of renal replacement therapy". Hemodialysis International. International Symposium on Home Hemodialysis. 10 Suppl 1 (Suppl 1): S19-23. doi:10.1111/j.1542-4758.2006.01185.x. PMID 16441862.
↑ Groothoff JW (July 2005). "Long-term outcomes of children with end-stage renal disease". Pediatric Nephrology. 20 (7): 849–53. doi:10.1007/s00467-005-1878-9. PMID 15834618.
↑ Giri M (2004). "Choice of renal replacement therapy in patients with diabetic end stage renal disease". EDTNA/ERCA Journal. 30 (3): 138–42. doi:10.1111/j.1755-6686.2004.tb00353.x. PMID 15715116.
↑ Pierratos A, McFarlane P, Chan CT (March 2005). "Quotidian dialysis--update 2005". Current Opinion in Nephrology and Hypertension. 14 (2): 119–24. doi:10.1097/00041552-200503000-00006. PMID 15687837.
↑ 69.0 69.1 Maisonneuve P, Agodoa L, Gellert R, Stewart JH, Buccianti G, Lowenfels AB, et al. (July 1999). "Cancer in patients on dialysis for end-stage renal disease: an international collaborative study". Lancet. 354 (9173): 93–9. doi:10.1016/S0140-6736(99)06154-1. PMID 10408483.
↑ American Society of Nephrology. "Five Things Physicians and Patients Should Question" (PDF). Choosing Wisely: An Initiative of the ABIM Foundation. Retrieved August 17, 2012.
↑ Chertow GM, Paltiel AD, Owen WF, Lazarus JM (June 1996). "Cost-effectiveness of cancer screening in end-stage renal disease". Archives of Internal Medicine. 156 (12): 1345–50. doi:10.1001/archinte.1996.00440110117016. PMID 8651845.
↑ Centers for Disease Control Prevention (CDC) (March 2007). "Prevalence of chronic kidney disease and associated risk factors--United States, 1999-2004". MMWR. Morbidity and Mortality Weekly Report. 56 (8): 161–5. PMID 17332726.
↑ Morgan T (21 January 2009). "Chronic Kidney Disease (stages 3–5) prevalence estimates using data from the Neoerica study (2007)". Association of Public Health Observatories.
↑ 74.0 74.1 74.2 Appel LJ, Wright JT, Greene T, Kusek JW, Lewis JB, Wang X, et al. (April 2008). "Long-term effects of renin-angiotensin system-blocking therapy and a low blood pressure goal on progression of hypertensive chronic kidney disease in African Americans". Archives of Internal Medicine. 168 (8): 832–9. doi:10.1001/archinte.168.8.832. PMC 3870204. PMID 18443258. [permanent dead link]
↑ "Tackling the £1.5bn a year cost of chronic kidney disease". Health Service Journal. 20 March 2020. Retrieved 16 May 2020.
↑ Lena, Pelander (2018). Chronic kidney disease in the dog. ISBN 978-91-7760-208-8. Retrieved 8 June 2018.
↑ Pelander L, Ljungvall I, Egenvall A, Syme H, Elliott J, Häggström J (June 2015). "Incidence of and mortality from kidney disease in over 600,000 insured Swedish dogs". The Veterinary Record. 176 (25): 656. doi:10.1136/vr.103059. PMID 25940343.
↑ "Olmesartan". clinicaltrials.
↑ "Angiotesin Receptor".
↑ Kim, Kun Hyung; Lee, Myeong Soo; Kim, Tae-Hun; Kang, Jung Won; Choi, Tae-Young; Lee, Jae Dong (2016-06-28). "Acupuncture and related interventions for symptoms of chronic kidney disease". The Cochrane Database of Systematic Reviews (6): CD009440. doi:10.1002/14651858.CD009440.pub2. ISSN 1469-493X. PMID 27349639.
ICD-10: N18
ICD-9-CM: 585.9 585.1-585.5 403
MedlinePlus: 000471
eMedicine: article/238798
Dialysis Complications of Chronic Renal Failure at eMedicine
Chronic Renal Failure Information from Great Ormond Street Hospital
Glomerular disease
See Template:Glomerular disease
Tubules
proximal
Gitelman syndrome
Liddle's syndrome
Interstitium
Balkan endemic nephropathy
Renal ischemia
Hypertensive nephropathy
Renovascular hypertension
Renal cortical necrosis
General syndromes
Nephrosis
Analgesic nephropathy
Renal osteodystrophy
Nephroptosis
Abderhalden–Kaufmann–Lignac syndrome
Nephrogenic
Renal papilla
Renal papillary necrosis
Major calyx/pelvis
Pyonephrosis
Organ failure
Multiple organ dysfunction syndrome
Retrieved from "https://mdwiki.org/w/index.php?title=Chronic_kidney_disease&oldid=352044"
CS1 errors: missing periodical
Articles with permanently dead external links
Articles lacking reliable references from April 2020


text:
Kent State reports 12 new COVID-19 cases, limits gatherings to 10 people
Krista S. Kano
Kent State University reported 12 new coronavirus cases for the week of Aug. 24 on Monday, bringing the total cases to 24 since July 7, with all cases occurring at the Kent campus.
The university also announced Monday that in-person classes will be the only gatherings where 10 or more people will be allowed based on guidance from the Kent City Health Department.
All university-sponsored events, meetings or gatherings of more than 10 people on the Kent campus must be held virtually, including events and activities sponsored by registered student organizations and academic departments.
"This is a precautionary and proactive measure to limit the spread of COVID-19 and to continue to maximize our opportunity to remain together on campus and learn in person. Currently, there is a small number of positive cases related to the Kent Campus," the university said in a statement.
Kent State students began moving into residence halls on Aug. 19, and classes began on Thursday.
The university also released its new coronavirus dashboard, which shows the number of cases at each of the eight campuses plus the College of Podiatric Medicine and the Twinsburg Academic Center. It will be updated weekly on Tuesdays.
The numbers represent outcomes from tests conducted at the DeWeese Health Center, as well as self-reported information from members of the Kent State community who have been tested at another location.
University spokesman Eric Mansfield was unable to provide further information about the positive cases, including whether they are faculty, staff or students; and whether the individuals live on or off campus. He was also unable to provide information regarding whether the university's dedicated isolation and quarantine spaces were currently in use.
Due to the low numbers, providing any information — including whether they are faculty, staff or students, whether they live on or off campus, or whether isolation and quarantine space is in use — may identify those individuals, Mansfield said.
Van Campen Hall, on the edge of Kent's campus, has been designated as isolation space for on-campus students who have tested positive for COVID-19. Additional rooms have been designated as quarantine space for those who may have been exposed to the disease, as determined by Kent Health, but have not yet tested positive.
Testing is available at the DeWeese Health Center and a new back-up trailer, and the university is offering Quest Diagnostics' COVID-19 self-collection test kits.
"The test kit was designed for self-collection by individuals with a consumer-friendly nasal swab approach. The test requires clinical observation when the individual does the test," Mansfield said.
The Kent Health Department is still in the process of conducting its contact tracing for the 12 new cases, Commissioner Joan Seidel said. There are currently 22 quarantined individuals in the city associated with Kent State's case, but there are more who are no longer in Kent, Seidel said.
"We're still in process. People will think about it and realize 'Oh I was with this person too,' so we don't get 100 percent of contacts on the first call," Seidel said.
She added that Kent State's coronavirus response team helps identify those who came in contact with the individuals who tested positive while on campus, but that the Health District takes a more "global approach" and looks at whom the individual may have come in contact with at off-campus jobs, restaurants or fitness classes.
"We've worked all through the summer together because not all students go home, so this is not a new relationship. We have an established relationship and we're working through the process to make sure it's as expedient as possible. We've got a good working relationship for sure," Seidel said.
Launched Monday, the dashboard also provides information about the status of each campus's classrooms, dining options, residence halls, research and work spaces. No changes have been made at any location.
According to an email sent Thursday by reopening committee chair Manfred van Dulmen, there is "not a magic number" that would initiate a change in campus operations.
Reporter Krista S. Kano can be reached at 330-541-9416, kkano@recordpub.com or on Twitter @KristaKanoRCedu.
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text:
Michael Jolley Has His Say After The Oldham Defeat
Club News 30 March 2019 3Views
"We're frustrated because in the first half, I thought we were definitely the better team," Jolley said.
"Second half, I think was more even, but they scored at important moments. It's very frustrating because we can't become a team that plays well and loses. It is very important that we refocus on the important moments in the game, which happen in both boxes. We have to do better with those."
The goals have dried up . . .
"I think it's a fair criticism that we're not scoring enough goals at the moment," he said. "We have to give that some very careful thought.
"When you don't win a game for a short time, or a while, you start to reflect on that.
"Are we creating enough good chances? Are we getting enough balls into the box? Are we getting enough people into the box? These are all things we need to think about, and we clearly have to do better.
"When you don't win a game for a while, you start to reflect on that, and that's what we're doing at the moment.
What are the gaffer's priorities between now and the end of the season – looking at players who are going to be here next season or winning games and finishing the season well?
Jolley added: "I think we had 750 supporters here, I just want to say thank you to them. I could hear them being supportive and positive right throughout the game. As the manager, that means a lot to us and we are very grateful and well done to them. I thought our supporters were brilliant today. They don't come to games expecting us to not win. I think we've got six games to go, we want to pick up more wins between now and the end of the season. Also, I'm looking at people within the squad and saying do you want to be part of this moving forward. ".
Listen to more from Michael Jolley for free on iFollow Mariners (above).
Town To Win And BTTS Now 9/1
Reserves In Action Today


text:
Q: Search and list items in vector Am working in J2ME where I have a field to search for items which is placed inside vectors. So I was wondering how to do it..? If suppose I have a 3 items starting with letter "A" then how would I print three of them..? I saw this and tried this
System.out.println("ITEM "+LIST_FNAM.indexOf(SEARCH_ITEM));

but the result was
ITEM 0

A: Assuming it is a Vector of Strings then you can do something like this:
for (String obj : vector) {
        if(obj.startsWith("A"))
           System.out.println(obj);
}

A: Using regular expression would be a nice choice if you want to implement searching.
You can put the entered string in a Regex and match it with the vector. It will help you in future if you want to enhance the searching capabilities like not just matching the first characters and finding the matched if they are in the middle of the patterns too. Saying that java provides a wonderful Regex matching support so implementing it won't be a much big issue also.

redpajama_set_name: RedPajamaStackExchange


In the northern hemisphere, we're entering winter when outside conditions may make photographing nature unpleasant. But that doesn't mean you should pack your camera up and wait for spring. Instead, investigate how window light can help you photograph nearly any subject.
All you need is a window (or door) with indirect light illuminating your subject. Window light is directional, revealing shape and texture, like that in the old cowboy hat above. Exposure times tend to be longer in this lighting situation, so using a tripod is helpful for a sharp shot without raising the ISO.
Learn more tips for using this natural light source indoors in Window Light Photography beginning November 27, 2018, in Missoula, Montana. Click here to register.


text:
Q: gzip: Interpreting bits for decompression I'm trying to learn the Inflate algorithm by implementing it in Java so that I may then implement it in assembly for a CPU with a very restricted instruction set.
I'm having trouble reading in the correct code lengths from the file after reading in the number of literal, distance, and length codes.
I'm following through an implementation as described here, where they provide an example .gz file gunzip.c.gz. After reading in the gzip headers, the following is the first 56 bits of the first (and if I'm reading it correctly, only) compressed data block:
10111101 00011011 11111101 01101111 11011010 11001000 11110010

I will refer to bits in a byte by the following offsets: [76543210]
The first byte 10111101 contains the end of block at offset 0, offset 21 contain the two bits that determine the block type.
In this case, this is the last block, and it is a dynamic Huffman Tree.
The following bits to be interpreted are the number of literal (5 bits), distance (5 bits), and length (4 bits) codes. They are read in as follows:
10111101 -> 10111XXX -> 23 (literal)
00011011 -> XXX11011 -> 27 (distance)
00011011 11111101 -> 000XXXXX XXXXXXX1 -> 1000 -> 8 (length)

After this point, I'm having trouble. The next 36 bits should be 12 sets of 3 bits that indicate the code lengths.
From the bytes above, I see (interpreted as little-endian):
110 111 111 011 011 010 011 011 100 100 101 100
3   7   7   6   6   2   6   6   1   1   5   1

But I expect (as indicated in the link above)
101 011 011 110 110 110 110 110 110 001 001 001
5   6   6   3   3   3   3   3   3   4   4   4

I can't see any way to get these values from the file. I must be misinterpreting how the bits should be read. Given a byte with a 5 bit value followed by a 3 bit value, [CBA43210] I would read it as 01234 and ABC.
Is the article wrong in what the correct code lengths should be, or more likely, am I wrong on how they should be interpreted?

A:
bits themselves are read LSB to MSB as illustrated in figure 6:
<----
87654321

(from the document linked by the question) indicates that

[CBA43210] I would read it as 01234 and ABC.

(from the question itself) is correct.
Little-endian means that least significant digits (here, bits) are stored or read (here, interpreted) first.
However, 01234 and ABC themselves are in little-endian, so the byte 110 11000 would be interpreted as 3 3, not 24 6.
This means the five, five and four bits in
10111101 00011011 ...

are
xxx11101 => 11101  => 29
101xxxxx
xxxxxx11 => 11 101 => 29
xx0110xx => 0110   => 6


pre-plumbed within a white powder coated aluminium panel with push button timed flow control and shower kit comprising chromium plated three function easy clean and flow regulated shower hand set with flexible hose and slide bar. Product Reference S407A as per drawing No. D10356.
The S407A is named on the Water Technology List (efficient showers) thus is eligible for Enhanced Capital Allowances (tax relief).